RANDOLPH M. MCCLOY, M.D.; WILLIAM P. BALDUS, M.D.; W. H. J. SUMMERSKILL, D.M.; FRANK T. MAHER, M.D., F.A.C.P.
Fluid retention accompanying advanced cirrhosis is characterized by secondary hyperaldosteronism and increased reabsorption of sodium by the kidney; the nature of the stimulus to increased aldosterone production is uncertain. The augmentation of aldosterone secretion in health resulting from infusion of angiotensin suggests that the latter may function as a trophic hormone for aldosterone (1-3). Whereas infusion of angiotensin causes sodium retention in normal man, patients with cirrhosis may exhibit a natriuretic and diuretic response (2). This paradoxical effect of angiotensin on sodium excretion in cirrhosis has not been explained. An opportunity to investigate the effects of angiotensin on renal function
MCCLOY RM, BALDUS WP, SUMMERSKILL WHJ, et al. Angiotensin-induced Natriuresis in Cirrhosis in the Absence of Endogenous Aldosterone Secretion. Ann Intern Med. 1966;64:1271–1276. doi: https://doi.org/10.7326/0003-4819-64-6-1271
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Published: Ann Intern Med. 1966;64(6):1271-1276.
DOI: 10.7326/0003-4819-64-6-1271
Gastroenterology/Hepatology, Liver Disease.
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